A simple presentation on hypokalemia. The most common electrolyte disorder in the Critical Care practice.The presentation is based on a mortality and morbidity case report and discussion. It covers all the basic aspects of understanding the causes of hypokalemia in ICU and its management. Target audience are residents ICU and ER but all health care workers can benefit.
This lecture is based on National guidelines(Sri Lanka) and guidelines by NHS UK. all the materials used to prepare the lecture are trusted and high in quality. also the books referred are internationally recognized. both hyper and hypokalemia management included in the lecture. lecture is free and you can even download. i kept no copy rights. i appreciate your support, comments and suggestions. also i would be grateful if you can make these lectures popular. wishing your success.
Potassium is the principal cation of the intracellular fl uid
(ICF) where its concentration is between 120 and 150 mEq/L.
The extracellular fl uid (ECF) and plasma potassium concentration [K] is much lower––in the 3.5–5.0 mEq/L range.
The very large transcellular gradient is maintained by active
K transport via the Na-K-ATPase pumps present in all cell
membranes and the ionic permeability characteristics of
these membranes. The resulting greater than 40-fold transmembrane [K] gradient is the principal determinant of the
transcellular resting potential gradient, about 90 mV with
the cell interior negative . Normal cell function
requires maintenance of the ECF [K] within a relatively narrow
range. This is particularly important for excitable cells
such as myocytes and neurons. The pathophysiologic effects
of dyskalemia on these cells result in most of the clinical
manifestations.
Acute kidney injury is common among hospitalized patients. It affects some 3–7% of patients admitted to the hospital and approximately 25–30% of patients in the intensive care unit.
A simple presentation on hypokalemia. The most common electrolyte disorder in the Critical Care practice.The presentation is based on a mortality and morbidity case report and discussion. It covers all the basic aspects of understanding the causes of hypokalemia in ICU and its management. Target audience are residents ICU and ER but all health care workers can benefit.
This lecture is based on National guidelines(Sri Lanka) and guidelines by NHS UK. all the materials used to prepare the lecture are trusted and high in quality. also the books referred are internationally recognized. both hyper and hypokalemia management included in the lecture. lecture is free and you can even download. i kept no copy rights. i appreciate your support, comments and suggestions. also i would be grateful if you can make these lectures popular. wishing your success.
Potassium is the principal cation of the intracellular fl uid
(ICF) where its concentration is between 120 and 150 mEq/L.
The extracellular fl uid (ECF) and plasma potassium concentration [K] is much lower––in the 3.5–5.0 mEq/L range.
The very large transcellular gradient is maintained by active
K transport via the Na-K-ATPase pumps present in all cell
membranes and the ionic permeability characteristics of
these membranes. The resulting greater than 40-fold transmembrane [K] gradient is the principal determinant of the
transcellular resting potential gradient, about 90 mV with
the cell interior negative . Normal cell function
requires maintenance of the ECF [K] within a relatively narrow
range. This is particularly important for excitable cells
such as myocytes and neurons. The pathophysiologic effects
of dyskalemia on these cells result in most of the clinical
manifestations.
Acute kidney injury is common among hospitalized patients. It affects some 3–7% of patients admitted to the hospital and approximately 25–30% of patients in the intensive care unit.
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
Knee anatomy and clinical tests 2024.pdfvimalpl1234
This includes all relevant anatomy and clinical tests compiled from standard textbooks, Campbell,netter etc..It is comprehensive and best suited for orthopaedicians and orthopaedic residents.
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
2. DEFINITION
It is defined as a serum potassium concentration greater than
5.5mEq/L.
The normal serum concentration range for potassium is 3.5-
5.0mEq/L
3. CAUSES OF HYPERKALEMIA :
I. Pseudohyperkalemia
II. Intra- to extracellular shift
III. Inadequate excretion
4. I. Pseudohyperkalemia
• Factitious hyperkalemia
•Artifactual increase in serum K+ due to the release of K+ during or after
venipuncture.
• Causes :
(a) In-vitro hemolysis.
(b) Marked leukocytosis or thrombocytosis
5. II. Intra- to extracellular shift
A. Acidosis
B. Hypertonicity
C. Digoxin and related glycosides (yellow oleander)
D. Succinylcholine; thermal trauma, neuromuscular injury, disuse
atrophy, mucositis, or prolonged immobilization
E. Rapid tumor lysis
6. (A) ACIDOSIS :
Acidemia → cellular uptake of H+ → efflux of K+
(B) HYPEROSMOLALITY
- Due to osmotic gradient ("solvent drag" effect)
-Hyperkalemia due to hypertonic mannitol, hypertonic saline, and
intravenous immune globulin is due to osmotic gradient.
-Diabetics are also prone to osmotic hyperkalemia in response to
intravenous hypertonic glucose, when given without adequate insulin.
7. (C) DIGOXIN
• Digoxin → inhibits Na+/K+-ATPase → impairs uptake of K+ so, digoxin
overdose → hyperkalemia.
• Structurally related glycosides found in yellow oleander or foxglove
8. • (D) SUCCINYLCHOLINE
• SCh → depolarizes muscle cells→ efflux of K+ through
acetylcholine receptors (AChRs).
• Contraindicated in patients who have sustained thermal
trauma, neuromuscular injury, disuse atrophy, mucositis, or
prolonged immobilization because it leads to an exaggerated
efflux of K+ causing acute hyperkalaemia.
9. (F) EXCESS INTAKE OR TISSUE NECROSIS
Following conditions provoke severe hyperkalemia in
susceptible patients :
Foods rich in potassium include tomatoes, bananas, and citrus
fruits;
Red cell transfusion, typically massive transfusions.
Finally, severe tissue necrosis, as in acute tumor lysis
syndrome and rhabdomyolysis.
10. • III. Inadequate excretion
A.Inhibition of RAAS; ↑ risk of hyperkalemia when used in combination :
ACE inhibitors, ARBs, Mineralocorticoidreceptor
blockers, Blockade of the ENaC
B. Decreased distal delivery eg., CHF
C. Hyporeninemic hypoaldosteronism
1. Tubulointerstitial diseases: SLE, sickle cell anemia
2. Diabetes, diabetic nephropathy
3. Drugs: NSAIDs, β-blockers, cyclosporine
4. Chronic kidney disease, advanced age
12. CLINICAL FEATURES
-Medical emergency due to its effects on heart, i.e., cardiac
arrhythmias.
Most of Hyperkalemic individuals are asymptomatic.
If present- symptoms are nonspecific and predominantly related to
muscular or cardiac functions.
The most common - weakness and fatigue.
Occasionally,frank muscle paralysis or shortness of breath.
Patients also may complain of palpitations or chest pain.
Arrythmias occur- Sinus Brady, Sinus arrest, VT, VF,
Asystole
Patients may report nausea, vomiting, and paresthesias
13. DIAGNOSTIC APPROACH
•First priority is to assess the need for emergency treatment, followed
by a comprehensive workup to determine the cause.
14.
15. Trans-tubular potassium gradient (TTKG) :
- index reflecting the conservation of potassium in the cortical
collecting ducts (CCD) of the kidneys.
17. TREATMENT :
The treatment of hyperkalemia is divided into three stages:
1.Immediate antagonism of the cardiac effects of hyperkalemia
- Intravenous calcium
2.Rapid reduction in plasma K+ concentration by redistribution
into cells
• Insulin
• β2-agonists (most commonly albuterol)
3. Removal of potassium
- using cation exchange resins, diuretics, and/or dialysis.
- Hemodialysis is the most effective and reliable method to reduce
plasma K+ concentration.
18.
19.
20.
21. Drugs Dosage ONSET
Length of MOA
effect
Cautions
Ca2+
gluconate
10 mL of
10% solution
IV over 10
minutes
Immediate 30 minutes
from toxic
effects of
Ca2+
Protects Can worsen
myocardium digoxin
toxicity
Insulin Regular
insulin 10
units IV with
50 mL of
50% glucose
15-30
minutes
2-6 hrs. Shifts K+ out
of the
vascular
space and
into the cells
Consider 5% Dextrose solution infusion at 100 mL/hr to prevent hypoglycemia
with repeated doses. Glucose unnecessary if blood sugar elevated above
250mg/dL
Albuterol
(Ventolin)
10-20 mg by
nebulizer
over 10
minutes (use
conc. form,
5mg/mL)
15-30 2-3 hrs.
minutes
Shifts K+
into the
cells,
additive to
the effect of
insulin
May cause a
brief initial
rise in
serum
potassium
22. Drugs Dosage Onset Length of
effect
MOA Cautions
Furosemide
(Lasix)
20-40 mg IV,
give with
saline if
volume
depletion is a
15 min. - 1
hr.
4 hrs. Increases
renal
excretion of
potassium
Only
effective if
adequate
renal
response to
concern loop diuretic
Sodium
polystyrene
sulfonate
(Kayexalate)
Oral : 50 g in
30 mL of
sorbitol
solution
Rectal : 50 g
in a retention
1-2 hrs.
(Rectal
route is
faster)
4-6 hrs. Removes
potassium
from the gut
in exchange
for sodium
Sorbitol may
be
associated
with Bowel
necrosis.
enema